Yunfei Zhang1, Hongyan Guo2, Hong Zhang2. 1. Deparetment of Pathology, the Affiliated Hospital of Northwest University for Nationalities, Second Province People's Hospital of Gansu, Lanzhou, 730000, Gansu, China. aowozhang754207@163.com. 2. Deparetment of Pathology, the Affiliated Hospital of Northwest University for Nationalities, Second Province People's Hospital of Gansu, Lanzhou, 730000, Gansu, China.
Abstract
BACKGROUND: The importance of long noncoding RNAs (lncRNAs) has been identified in human cancers, such as emerged as tumor facilitator or tumor suppressor. Small nucleolar RNA host gene 10 (SNHG10) has been reported as an oncogenic lncRNA in hepatocellular carcinoma. However, its functional role and underlying mechanism in gastric cancer (GC) need to be further explored. AIMS: Our study was conducted to investigate the function and molecular mechanism of SNHG10 in GC. METHODS: SNHG10 expression was detected by qRT-PCR. The effect of SNHG10 on GC cell growth was assessed by colony formation, EdU, JC-1, flow cytometry, and wound-healing assays. The interaction between SNHG10 and PBX3 was confirmed through ChIP and luciferase reporter assay. RIP and RNA pull down assays was used to define the binding of DEAD-box helicase 54 (DDX54) to SNHG10 or PBX homeobox 3 (PBX3). RESULTS: SNHG10 was expressed at a high level in GC cells. SNHG10 knockdown resulted in the inhibition on GC cell proliferation, migration but induced cell apoptosis. PBX3 could interact with SNHG10 promoter and thereby activate the expression of SNHG10. Subsequently, it was confirmed that SNHG10 positively modulated the expression of PBX3. Based on this, we found that DDX54 could bind to SNHG10 and PBX3, suggesting that SNHG10 maintained PBX3 mRNA stability through recruiting DDX54. Restoration assays indicated that PBX3 overexpression recovered SNHG10 silencing-induced inhibition on GC cell growth. CONCLUSIONS: SNHG10 facilitates cell growth by affecting DDX54-mediated PBX3 mRNA stability in GC.
BACKGROUND: The importance of long noncoding RNAs (lncRNAs) has been identified in human cancers, such as emerged as tumor facilitator or tumor suppressor. Small nucleolar RNA host gene 10 (SNHG10) has been reported as an oncogenic lncRNA in hepatocellular carcinoma. However, its functional role and underlying mechanism in gastric cancer (GC) need to be further explored. AIMS: Our study was conducted to investigate the function and molecular mechanism of SNHG10 in GC. METHODS: SNHG10 expression was detected by qRT-PCR. The effect of SNHG10 on GC cell growth was assessed by colony formation, EdU, JC-1, flow cytometry, and wound-healing assays. The interaction between SNHG10 and PBX3 was confirmed through ChIP and luciferase reporter assay. RIP and RNA pull down assays was used to define the binding of DEAD-box helicase 54 (DDX54) to SNHG10 or PBX homeobox 3 (PBX3). RESULTS: SNHG10 was expressed at a high level in GC cells. SNHG10 knockdown resulted in the inhibition on GC cell proliferation, migration but induced cell apoptosis. PBX3 could interact with SNHG10 promoter and thereby activate the expression of SNHG10. Subsequently, it was confirmed that SNHG10 positively modulated the expression of PBX3. Based on this, we found that DDX54 could bind to SNHG10 and PBX3, suggesting that SNHG10 maintained PBX3 mRNA stability through recruiting DDX54. Restoration assays indicated that PBX3 overexpression recovered SNHG10 silencing-induced inhibition on GC cell growth. CONCLUSIONS: SNHG10 facilitates cell growth by affecting DDX54-mediated PBX3 mRNA stability in GC.